The invention relates generally to the field of medical devices, specifically to medical devices that are useful in treating stroke, and more particularly to a device allowing for the flow of oxygenated blood through an obstructed artery thus sustaining at least partial patency.
Stroke is a leading cause of disability, death and health care expenditure. Most strokes are ischemic, i.e. caused by a decrease in the blood supply to a portion of the brain due to a clot obstructing the flow of blood. A total or hemodynamically significant occlusion of a cerebral artery in an acute ischemic stroke is mostly due to thrombus formation, an embolus, and/or other unwanted matter. When an artery is obstructed, tissue ischemia (lack of oxygen and nutrients) quickly develops. The organ most sensitive to ischemia is the brain. Ischemia will rapidly progress to tissue infarction (cell death) if the occlusion of blood flow persists. In patients experiencing a typical large vessel acute ischemic stroke, it has been estimated that within each hour of no cerebral perfusion, about 20 million neurons are lost. Therefore, cerebral artery occlusions that lead to stroke require swift and effective therapy to reduce the morbidity associated with the disease. The term occlusion as used herein is meant to include any partial or complete blockage of a blood vessel, as by thrombosis, embolism or gradual narrowing.
The functionally impaired region that surrounds the infarct core and is threatened by cell death has been termed the ischemic penumbra. The ischemic penumbra, although physiologically impaired, is potentially salvageable tissue, however the window of opportunity for recovery of the reversibly injured neurons in the ischemic penumbra is relatively short. Failure to timely restore blood flow triggers a biochemical and metabolic cascade ultimately leading to irreversible brain injury by progressive transformation of the ischemic penumbra into infarcted tissue, i.e. the infarct core expands as the penumbra tissue experiences necrosis.
Traditionally, emergency management of acute ischemic stroke consisted of mainly general supportive care, e.g. hydration, monitoring neurological status, blood pressure control, and/or anti-platelet or anti-coagulation therapy. In 1996 intra-arterial administration of tissue plasminogen activator (t-PA) was approved by the FDA for the treatment of acute ischemic stroke in selected cases within the first few hours from onset. More recently percutaneous catheter-based technologies have been advanced, including: placing a microcatheter near the clot and infusing a thrombolytic agent in order to dissolve the clot; extracting the clot by distal embolectomy devices in which various wire corkscrews and baskets are advanced distally through the clot in order to capture it; and using proximal devices in which the clot is aspirated or captured and removed. Other methods of removing or disrupting the clot, include: facilitating fibrinolysis by an outside energy source such as ultrasound or laser energy; mechanical manipulation of the clot by primary angioplasty; and employing stents permanently or transiently are also widely used.
Often, more than one method is required until arterial patency is restored. Such treatment approaches have a common purpose of restoring artery patency as quickly as possible by removing or disrupting the obstructing clot. Achieving artery patency by any of these above methods or any combination of them (multimodal therapy) is often complex, requires multiple steps and is time consuming. Even if the treatment is successful, during the treatment progressive transformation of the penumbra into infarcted tissue occurs.
A key therapeutic goal of acute ischemic stroke treatment consists of re-establishment of arterial potency prior to cell death. The sooner arterial patency is achieved the greater the clinical benefit, therefore early restoration of blood flow in the affected territory of the brain may save brain tissue.
Cells within an infarction zone have dramatically reduced blood flow to less than 20% of normal blood flow. As a result, cells within this infarction zone will be irreversibly damaged within a few minutes. The blood flow in the ischemic penumbra, surrounding the infarction zone, is between 20% and 50% of normal. Cells in this area are endangered, but not irreversibly damaged. Studies have indicated that a critical focal stenosis of ˜75% decrease in diameter is usually required to compromise flow in a major cerebral artery, in face of insufficient collateral flow from other arteries.
U.S. Patent Application Publication S/N 2007/0208367 published Sep. 6, 2007 to Fiorella et al is directed to a method of increasing blood flow through an obstructed blood vessel includes providing an expandable member substantially made of a mesh having a plurality of interstices. The expandable member is expanded to bring at least a portion of the member body into contact with the occlusion. An outward radial force is exerted on the occlusion to dislodge at least one fragment from the occlusion and to enhance blood flow through the blood vessel past the occlusion. Disadvantageously, the radial force required may traumatize the blood vessel exhibiting the occlusion. A means for capturing the dislodged fragment is provided, however the blood flow interruption due to the capturing mesh itself induces flow resistance. Additionally, aggregation of the dislodged fragments in the capturing mesh disrupts and subsequently decreases the blood flow.
U.S. Pat. No. 6,295,990 issued Oct. 2, 2001 to Lewis et al, the entire contents of which is incorporated herein by reference, is addressed to methods for treating total and partial occlusions by employing a perfusion conduit which is penetrated through the occlusive material. Oxygenated blood or other medium is then perfused through the conduit in a controlled manner, preferably at a controlled pressure below the arterial pressure, to maintain oxygenation and relieve ischemia in tissue distal to the occlusion. The device and method of Lewis is based on an elongated solid catheter extending from outside the patient body until penetrating the occlusion. In an embodiment in which passive perfusion is implemented, blood inlet ports are provided near the proximal end with blood outlet ports provided at the distal end. The requirement for inlet and outlet ports fails to take full advantage of the pressure differential between the proximal and distal sides of the occlusion.
An article by Kelly et al published in Stroke, June 2008 at pages 39: 1770-1773 entitled “Recanalization of an Acute Middle Cerebral Artery Occlusion Using a Self-Expanding, Reconstrainable, Intracranial Microstent as a Temporary Endovascular Bypass is addressed to providing a temporary bypass using a self expanding stent. Disadvantageously, the self expanding stent exerts radial force against the occlusion, which may result in undesired breaking up of the occlusion with significant fragments being dislodged to proceed further into the bloodstream resulting in potential brain damage.
There is thus a need for a method and apparatus for passively perfusing oxygenated blood through an obstructing clot while minimizing undesired radial force against the occlusion.